Archive for May, 2014

Study: Herbal Mixture Provides Significant Results for Children with RLS

ImageIn the following study from 2005, researchers created a mixture of several healing ingredients and produced a syrup which the children with RLS took orally.

Out of the 14 ingredients in the mixture, 13 of them had ANTI-INFLAMMATORY properties (references can be found for each by following the link at the end of this post). The only ingredient that didn’t have anti-inflammatory properities was Long Gu (Dragon’s Bone) which is “ground bone” – a sedative to reduce stress and calm the mind.


“Fifty cases of child restless legs syndrome treated with the integrated method of Chinese Herbal drugs.”
Wang W. and Fan H. J Tradit Chin Med. 2005 Dec;25(4):276-7.

Fifty cases of child restless syndrome were treated with oral administration of Chinese traditional herbal drugs plus auricular-plaster therapy from December 1998 to November 2001, and another 47 cases were treated with oral administration of methylphenidate as controls


For patients in the treatment group the ingredients of formula were prescribed as below:  Image

Fu-Ling (Poria cocos) 40g
Shan Yao / Radix Dioscoreae (Chinese Yam Root) 40g
Radix Rehmanniae Praeparata 30g
Shan Zhu Yu (Fructus Corni) 30g
Shi Chang Pu (Rhizoma Acori Tatarinowii) 45g
Yuan Zhi / Radix Polygalae (Chinese Senega Root) 30g
Bai Ji Li (Fructus Tribuli) 30g
Long Gu (Dragon’s Bone) 60g
Mu Li (Oyster shell) 60g
Jiang Can / Bombyx Batryticatus (Silkworm) 30g
Gou Teng (cat’s claw) 30g
Yi Zhi Ren (Chinese Ginger) 30g
Da Zao (Jujube Fruit) 30g
Gan Cao / Radix Glycyrrhizae (Licorice Root) 25g   

They were made into 250 ml of syrup in the pharmaceutics department of this hospital.

The syrup was orally administered to the patients under 9 years in a dose of 25 ml, three times daily, and to the patients over 9 years in a dose of 40 ml, three times daily.


Of the 50 cases in the treatment group, 21 cases were markedly effective, 26 cases effective, and 3 cases ineffective, with a total effective rate of 94%. Among the 47 cases in the control group, 15 cases were markedly effective, 17 cases effective, and 15 cases ineffective, with a total effective rate of 68.09%. The difference in total effective rate between the two groups was statistically very significant (P<0.01).


The results showed that the therapeutic effect of the treatment group was significantly superior to that of the control group

For details on the anti-inflamatory properties of the ingredients please visit:

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Successful Treatment of Restless Legs Syndrome with the Herbal Prescription “Yokukansan.”

ImageYokukansan, also known as TJ-54, is composed of SEVEN herbs; Angelica acutiloba, Atractylodes lancea, Bupleurum falcatum, Poria cocos, Glycyrrhiza uralensis, Cnidium officinale and Uncaria rhynchophylla.

Yokukansan is used to treat insomnia and irritability as well as screaming attacks, sleep tremors and hypnic myoclonia, and neurological disorders which include dementia and Alzheimer’s disease.

Not only has Yokukansan proven in studies to have STRONG anti-inflammatory qualities, but EACH of the seven herbs that make up Yokukansan have anti-inflammatory qualities (references to these studies are below).

In 2010 a study showed that Yokukansan was beneficial in relieving RLS in all 3 test subjects.

In their conclusion, the scientists don’t mention that it was due to the anti-inflammatory properties of Yokukansan that brought on the relief in all 3 subjects.

However, it is just a matter of time before this case becomes another obvious example of the undeniable LINK between inflammation and RLS.

“Successful treatment of restless legs syndrome with the herbal prescription Yokukansan.”

Hideto Shinno, Mami Yamanaka, Ichiro Ishikawa, Sonoko Danjo, Yasushi Inami, Jun Horiguchi and Yu Nakamura. Progress in Neuro-Psychopharmacology and Biological Psychiatry. Volume 34, Issue 1, 1 February 2010, Pages 252–253.


RLS improved in ALL 3 cases after the addition of Yokukansan. We speculate that actions on GABAergic, serotonergic and dopaminergic systems might account for some of the therapeutic effects of KS in the present cases. YKS, therefre, appears to be useful in RLS treatment.


“Use of Yokukansan (TJ-54) in the treatment of neurological disorders: A review.”
S. de Caires, V. Steenkamp. Department of Pharmacology, Faculty of Health Sciences, University of Pretoria

“Ameliorative effects of yokukansan on behavioral deficits in a gerbil model of global cerebral ischemia.”
Liu Y et al. Brain Res. 2014 Jan 16;1543:300-7. doi: 10.1016/j.brainres.2013.11.015. Epub 2013 Nov 19.

“Yokukansan promotes hippocampal neurogenesis associated with the suppression of activated microglia in Gunn rat.”
Motohide Furuya et al. Journal of Neuroinflammation 2013, 10:145 doi:10.1186/1742-2094-10-145

“Effects of Angelica acutiloba on mast cell-mediated allergic reactions in vitro and in vivo.”
Kyungjin Lee et al. Immunopharmacology and Immunotoxicology, August 2012, Vol. 34, No. 4 : Pages 571-577

“Further Phenols and Polyacetylenes from the Rhizomes of Atractylodes lancea and their Anti-Inflammatory Activity.”
M. Resch et al. Planta Med 2001; 67(5): 437-442. DOI: 10.1055/s-2001-15817

Bupleurum (Bupleurum falcatum)

Assessment of anti-inflammatory activity of Poria cocos in sodium lauryl sulphate-induced irritant contact dermatitis.
Fuchs SM et al. Skin Res Technol. 2006 Nov;12(4):223-7.

“Antioxidant and Antiinflammatory Activities of Licorice Root (Glycyrrhiza uralensis): Aroma Extract.”
Aki Tanaka and Takayuki Shibamoto. Chapter 20, pp 229–237. Chapter DOI: 10.1021/bk-2008-0993.ch020. ACS Symposium Series, Vol. 993.

“Components of rhizome extract of Cnidium officinale Makino and their in vitro biological effects.”
Bae KE et al. Molecules. 2011 Oct 21;16(10):8833-47. doi: 10.3390/molecules16108833.

“Uncaria rhynchophylla inhibits the production of nitric oxide and interleukin-1ß through blocking nuclear factor ?B, Akt, and mitogen-activated protein kinase activation in macrophages.”
Kim JH et al. J Med Food. 2010 Oct;13(5):1133-40. doi: 10.1089/jmf.2010.1128.

You can read the full study here:

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Studies Show that Stress Increases Inflammation Levels

ImageMy last post featured studies on how INSOMNIA increases inflammation. This post will examine how STRESS increases inflammation.

If you’ve read some of the posts on this page, or have visited my website – you’ll know that I FIRMLY believe that inflammation is the CAUSE of RLS. Science is now confirming this.

What this means is that insomnia and stress are issues that must somehow be dealt with in order to help your suffering to come to an end. The MORE the inflammation in your body increases, the MORE your legs will act up.

Prescribed drugs are not the answer. Whatever lies beneath the surface and is causing your stress cannot be dissolved with a drug. That requires change through meditation, relaxation exercises, therapy etc.

This post provides scientific evidence that stress increases inflammation levels.

The information you’ll read below are short excerpts from articles talking about the studies. To view the full studies please visit:stressedcake

“Chronic Stress Changes Immune Cell Genes, Leading To Inflammation” Huffington Post, July 7, 2013

A new study provides a better understanding of why chronic stress leads to high levels of inflammation in the body.

Researchers found that chronic stress changes gene activity of immune cells before they enter the bloodstream so that they’re ready to fight infection or trauma — even when there is no infection or trauma to fight. This then leads to increased inflammation.

“Dwelling on stressful events can increase inflammation in the body, study finds.” Ohio University Office of Research Communications. March 13, 2013.

Dwelling on negative events can increase levels of inflammation in the body, a new Ohio University study finds.

Researchers discovered that when study participants were asked to ruminate on a stressful incident, their levels of C-reactive protein, a marker of tissue inflammation, rose. The study is the first to directly measure this effect in the body.

Image“How Stress Influences Disease: Carnegie Mellon Study Reveals Inflammation as the Culprit.” Carnegie Mellon News (April 2012).

A research team led by Carnegie Mellon University’s Sheldon Cohen has found that chronic psychological stress is associated with the body losing its ability to regulate the inflammatory response. Published in the Proceedings of the National Academy of Sciences, the research shows for the first time that the effects of psychological stress on the body’s ability to regulate inflammation can promote the development and progression of disease.

“Inflammation is partly regulated by the hormone cortisol and when cortisol is not allowed to serve this function, inflammation can get out of control,” said Cohen, the Robert E. Doherty Professor of Psychology within CMU’s Dietrich College of Humanities and Social Sciences.

Cohen argued that prolonged stress alters the effectiveness of cortisol to regulate the inflammatory response because it decreases tissue sensitivity to the hormone. Specifically, immune cells become insensitive to cortisol’s regulatory effect. In turn, runaway inflammation is thought to promote the development and progression of many diseases.

“When under stress, cells of the immune system are unable to respond to hormonal control, and consequently, produce levels of inflammation that promote disease. Because inflammation plays a role in many diseases such as cardiovascular, asthma and autoimmune disorders, this model suggests why stress impacts them as well.”

“Brain pathways linking social stress and inflammation identified.” from Science Daily. Aug. 2010.

A new studys show that individuals who exhibit greater neural sensitivity to social rejection also exhibit greater increases in inflammatory activity to social stress.2stress

Their results showed that individuals who exhibited greater neural activity in the dorsal anterior cingulate cortex and anterior insula during social rejection in the brain scanner also exhibited greater increases in inflammatory activity when exposed to acute social stress in the lab.

“This is further evidence of how closely our mind and body are connected,” Slavich said. “We have known for a long time that social stress can ‘get under the skin’ to increase risk for disease, but it’s been unclear exactly how these effects occur. To our knowledge, this study is the first to identify the neurocognitive pathways that might be involved in inflammatory responses to acute social stress.”


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Studies Show that Insomnia Increases Inflammation Levels

ImageYou’re lying awake in bed at 4 am. – it’s another sleepless night. Your legs are twitching and pulsating, your mind is racing aimlessly with blurred abstract nonsense and the giant purple bags under your eyes continue to darken and grow larger.

Yes, we’ve all been there.

The last thing you need to hear is that your STRESS and LACK OF SLEEP are actually making the problem WORSE!

But, it’s the truth.

And now that you know this, you can do something about it.

As the powerful influence of inflammation continues to move to the forefront of the media, more and more studies are being done to find out just how widespread its effects are. This includes studies I’ll present to you on this website showing that both stress and insomnia increase inflammation levels.

This post provides scientific evidence that insomnia increases inflammation levels. My next post will focus on how stress increases inflammation levels.

The information you’ll read below are short excerpts from the studies. To view the full studies please visit:

Image“Sleep Loss and Inflammation.”
Janet M. Mullington et al. Best Pract Res Clin Endocrinol Metab. Oct 2010; 24(5): 775–784.


Controlled, experimental studies on the effects of acute sleep loss in humans have shown that mediators of inflammation are altered by sleep loss.  


“Sleep duration and biomarkers of inflammation.”
Patel SR et al. Sleep. 2009 Feb;32(2):200-4.


Extremes of sleep duration have been associated with adverse health outcomes. The mechanism is unclear but may be related to increased inflammation. We sought to assess the association between sleep duration and inflammatory biomarkers.


Increases in habitual sleep durations are associated with elevations in CRP and IL-6 while reduced PSG sleep duration is associated with elevated TNFa levels. Activation of pro-inflammatory pathways may represent a mechanism by which extreme sleep habits affect health.

Image“Sleep Loss Activates Cellular Inflammatory Signaling”
Michael R. Irwin et al. Biol Psychiatry. 2008 Sep 15;64(6):538-40.


Accumulating evidence suggests that sleep disturbance is associated with inflammation and related disorders including cardiovascular disease, arthritis, and diabetes mellitus. This study was undertaken to test the effects of sleep loss on activation of nuclear factor (NF)-kappaB, a transcription factor that serves a critical role in the inflammatory signaling cascade.


“Chronic Insomnia and Stress System.”
Maria Basta, M.D. et al. Sleep Med Clin. Jun 2007; 2(2): 279–291.


In insomnia, which is a very common sleep disorder, objective sleep measures, EEG activity, physiologic findings, HPA axis activity and inflammation markers suggest that it is not a state of sleep loss, but a disorder of hyperarousal present both during the night and the daytime.

The finding that pro-inflammatory cytokines’ IL-6 and TNFa daytime secretion is elevated in insomniacs, considering their role in subjective complaints of fatigue and poor performance, may lead to novel approaches to treat insomnia.


“The effects of 40 hours of total sleep deprivation on inflammatory markers in healthy young adults.”
Frey DJ et al. Brain Behav Immun. 2007 Nov;21(8):1050-7.


Inflammatory cytokines are released in response to stress, tissue damage, and infection. Acutely, this response is adaptive; however, chronic elevation of inflammatory proteins can contribute to health problems including cardiovascular, endocrine, mood, and sleep disorders.

Our findings suggest that one night of sleep loss triggers a stress response that includes stimulation of both pro- and anti-inflammatory proteins in the healthy young subjects tested under our experimental conditions.


“Effect of sleep loss on C-reactive protein, an inflammatory marker of cardiovascular risk.”Image
Meier-Ewert HK et al. J Am Coll Cardiol. 2004 Feb 18;43(4):678-83.


Both acute total and short-term partial sleep deprivation resulted in elevated high-sensitivity CRP concentrations, a stable marker of inflammation that has been shown to be predictive of cardiovascular morbidity. We propose that sleep loss may be one of the ways that inflammatory processes are activated and contribute to the association of sleep complaints, short sleep duration, and cardiovascular morbidity observed in epidemiologic surveys.


“Sleep Restriction Increases the Risk of Developing Cardiovascular Diseases by Augmenting Proinflammatory Responses through IL-17 and CRP.”
Wessel M. A. et al. PLoS One. 2009;4(2):e4589. doi: 10.1371/journal.pone.0004589. Epub 2009 Feb 25.


Sleep restriction, leading to deprivation of sleep, is common in modern 24-h societies and is associated with the development of health problems including cardiovascular diseases. Our objective was to investigate the immunological effects of prolonged sleep restriction and subsequent recovery sleep, by simulating a working week and following recovery weekend in a laboratory environment.


5 nights of sleep restriction increased lymphocyte activation and the production of proinflammatory cytokines including IL-1beta IL-6 and IL-17; they remained elevated after 2 nights of recovery sleep, accompanied by increased heart rate and serum CRP, 2 important risk factors for cardiovascular diseases. Therefore, long-term sleep restriction may lead to persistent changes in the immune system and the increased production of IL-17 together with CRP may increase the risk of developing cardiovascular diseases.

For tips on putting an end to your sleepless nights, please visit these pages:


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How Inflammation Can Affect Iron Levels

ImageThere are hundreds of articles parroting each other on the internet talking about what causes Restless Legs Syndrome. The two most agreed upon theories are an imbalance of dopamine (a chemical that transmits signals between nerve cells in the brain) and low iron levels.

I’m going to present evidence that both of these conditions could be caused by the presence of inflammation. In other words, I believe inflammation to be the primary condition while restless legs, dopamine imbalance and low irons levels are simply effects of this chronic state.

This post provides scientific evidence that inflammation can affect iron/ferritin levels.

For information on how inflammation can affect dopamine levels, please visit

from Stop The Thyroid Madness “Iron and hypothyroidism”

Ferritin is an iron-storage protein which keeps your iron in a dissolvable and usable state, making the iron non-toxic to cells around it. So when Ferritin is measured via a blood test, it is basically measuring the iron you have tucked away for safe use. 70 – 90 is often mentioned in literature as a goal, but other iron labs are important with it, as your ferritin can look good, but your other labs reveal the truth. Inflammation tends to thrust iron into storage, so you can’t just look at Ferritin.

Inflammation can lower your iron levels. If you are having a hard time raising iron, or keeping it up, you may also have a chronic inflammation problem that needs discovery and treatment. Gluten can cause inflammation for those with Hashi’s. Even without Hashi’s, thyroid patients can have chronic inflammation in their joints. An allergy to what you eat can cause inflammation, as happened to thyroid patient Deb who discovered she was allergic to eggs. Once she removed eggs, her iron went up!

from “Towards explaining ‘unexplained’ hyperferritinemia” by Clara Camaschella and Erika Poggiali

It is well known that both acute and chronic inflammation, as occurring in infections, autoimmune disorders, chronic renal failure and also cancer – all conditions common in hospitalized patients – are associated with high ferritin levels.

Imagefrom WEB MD “Ferritin”

Reasons you may not be able to have the ferritin test or why the results may not be helpful include:

Having a blood transfusion in the past 4 months.
Being a female athlete whose amount of activity has changed her menstrual cycle.
Having conditions that cause inflammation in the body, such as from illness or from a surgery.
Having a radioactive scan in the past 3 days.
Taking medicines, such as birth control pills and antithyroid medicines.
Age. Older adults may have a higher ferritin value.
Eating a diet high in red meats.

Because inflammation in the body can cause high ferritin levels, a test result that is slightly high does not always mean a buildup of iron (hemochromatosis) is present.

from “Interpretation of biochemical tests for iron deficiency: diagnostic difficulties related to limitations of individual tests”
by Frank Firkin, Director of Clinical Haematology; and Bryan Rush, Director of Laboratory Haematology, St Vincent’s Hospital, Melbourne.


The results of tests of iron status are relatively frequently distorted by other clinical factors. This is important to recognise as such distorted results may give a misleading view of the patient’s iron stores. The impact of these factors can be recognised by combining the results of currently available tests.


Most cases of iron deficiency can be diagnosed with simple tests. The concentration of serum iron does not fall until the body’s iron stores are exhausted. As the stores are depleted, the concentration of transferrin rises while the concentration of ferritin falls.

Caution is required when assessing patients with inflammatory disease as a low serum iron may not represent iron deficiency. These patients often have reduced concentrations of transferrin.

Imagefrom “Influence of acute inflammation on iron and nutritional status indexes in older inpatients.”
Chiari MM1, Bagnoli R, De Luca PD, Monti M, Rampoldi E, Cunietti E. J Am Geriatr Soc. 1995 Jul;43(7):767-71.


To investigate the relations between acute inflammation, as shown by high C-reactive protein (CRP) serum levels, and laboratory indexes of iron and nutritional status and to ascertain whether the presence of acute inflammation affects the diagnostic reliability of these indexes.


Patients with acute inflammation present altered iron status indexes that resemble those observed in the anemia of chronic disease.

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A 2014 Study Indicates that there is a Direct Link Between Restless Legs Syndrome and Inflammation

ImageInterleukin-17A is a protein that in humans is encoded by the IL17A gene. The protein encoded by this gene is a proinflammatory cytokine produced by activated T cells.
“IL17A” Wikipedia

As you will read below in the OBJECTIVE of Dr. Hennessey’s study, dopamine, iron and inflammatory pathways are considered important to the development of RLS.

My belief, as I’ve stated and provided evidence for on my website (links below) is that it is the inflammation that is affecting the dopamine and iron levels in RLS sufferers  – as well as creating the uncomfortable sensations in the legs.

At the very least, what you can take out of this study is that inflammation is now being directly linked to RLS by scientists. There are many other factors that need to be explored in the scientific community, but they are now at least agreeing, due to the growing body of evidence, that inflammation a primary component.

Here is the study:

 “Polymorphisms of Interleukin-1 Beta and Interleukin-17 Alpha Genes Are Associated With Restless Legs Syndrome.”
by Mary Dawn Hennessy, RN, PhD, Rochelle S. Zak, MD, Caryl L. Gay, PhD, Clive R. Pullinger, Kathryn A. Lee, RN, PhD and Bradley E. Aouizerat, MAS, PhD.  Biol Res Nurs April 2014 vol. 16 no. 2 143-151. doi: 10.1177/1099800413478827  


Dopamine, iron, and inflammatory pathways are considered important to the development of restless legs syndrome (RLS). Recent genetic studies support involvement of dopamine and iron; however, cytokine gene variation in the inflammatory component remains unexplored. A recent study reported a high prevalence of RLS among HIV-infected adults. We estimate occurrence of RLS in an ethnically diverse sample of HIV-infected adults and examine differences in demographic factors, clinical characteristics, and biomarkers relating to dopamine, iron, and inflammation between adults with and without RLS symptoms. Design: A prospective longitudinal study aimed at identifying biomarkers of RLS symptom experience among HIV-infected adults.


316 HIV-positive adults were evaluated using International RLS Study Group criteria. Genes were chosen for hypothesized relationships to dopamine (NOS1, NOS2), iron (HFE) or inflammation-mediated by cytokine genes (interferon [IFN], interleukin [IL], nuclear factor kappa-B [NFKB], and tumor necrosis factor alpha [TNFA]).


Similar to general population estimates, 11% of the sample met all four RLS diagnostic criteria. Controlling for race, gender, and hemoglobin, carrying two copies of the minor allele for IL1B rs1143643, rs1143634, or rs1143633 or carrying the minor allele for IL17A rs8193036 was associated with increased likelihood of meeting RLS diagnostic criteria.


This study provides preliminary evidence of a genetic association between IL1B and IL17A genes and RLS.

You can read the study here:

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A 2012 Study Shows that there is a Link Between Restless Legs Syndrome and Inflammation

ImageFor 5 years now I’ve been collecting data to help support my claim that RLS is caused by inflammation. The evidence is overwhelming, but still the willingness by anyone to make the required lifestyle changes to lessen their RLS is a rare occurrence. The pharmacological solution still rules.

There are countless stories of people that have become free of their RLS through various natural methods. These methods (as I indicate on my website) always have an anti-inflammatory component to them.

Unfortunately this body of evidence will always be considered “anecdotal” in the eyes of scientists. We’re simply children entertaining the grownups with our wild imagination.

Scientists build truths based solely upon the studies of their peers. That’s the ONLY data that they will consider.

This is why Dr. Weinstock’s study on the relationship between RLS and inflammation was such a groundbreaking event. Even though Dr. Weinstock will not be continuing with further studies of the relationship between RLS and inflammation (due to a lack of funding) others are expanding on his findings.

That includes a study (below) that I just ran across. It was originally published in the Nov. 2012 edition of the scientific journal “Brain, Behavior and Immunity.”

The study clearly demonstrates that there is a direct correlation between elevated C-reactive protein (an indicator of inflammation) and Restless Legs Syndrome.

Here is the study …

Image“Elevated C-reactive protein is associated with severe periodic leg movements of sleep in patients with restless legs syndrome.”
by Lynn Marie Trotti, Rye DB, De Staercke C, Hooper WC, Quyyumi A, Bliwise DL. Brain Behav Immun. 2012 Nov;26(8):1239-43. doi: 10.1016/j.bbi.2012.06.003. Epub 2012 Jun 26. Emory Program in Sleep, Department of Neurology, Emory University School of Medicine, Atlanta, GA



Restless legs syndrome (RLS) is a common sleep disorder in which urges to move the legs are felt during rest, are felt at night, and are improved by leg movement. RLS has been implicated in the development of cardiovascular disease. Periodic leg movements (PLMs) may be a mediator of this relationship. We evaluated systemic inflammation and PLMs in RLS patients to further assess cardiovascular risk.


137 RLS patients had PLM measurements taken while unmedicated for RLS. Banked plasma was assayed for high sensitivity C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF-alpha).


Mean (SD) PLM index was 19.3 (22.0). PLMs were unrelated to TNF-a and IL-6, but were modestly correlated with logCRP (r(129)=0.19, p=0.03). Those patients with at least 45PLMs/h had an odds ratio of 3.56 (95% CI 1.26-10.03, p=0.02, df=1) for having elevated CRP compared to those with fewer than 45PLMs/h. After adjustment for age, race, gender, diabetes, hypertension, hyperlipidemia, inflammatory disorders, CRP-lowering medications, and body mass index, the OR for those with ≥ 45PLMs/h was 8.60 (95% CI 1.23 to 60.17, p=0.03, df=10).


PLMs are associated with increased inflammation, such that those RLS patients with at least 45PLMs/h had more than triple the odds of elevated CRP than those with fewer PLMs. Further investigation into PLMs and inflammation is warranted.

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